Polyneuropathy associated with IgM monoclonal gammopathy

Vital, Anne; Vital, C; Julien, Jean-Philippe; Baquey, A.; Steck, Andreas

doi:10.1007/bf00294374

Cited by 121 publications

(13 citation statements)

References 29 publications

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“…In contrast, another describes extensive proliferation of lymphoplasmacytoid B cells in the epineurium, perineurium and endoneurium ( Kanda et al, 1998 ) , which were not present in our case. There were no features in our patient of proliferative endothelial microangiopathy ( Vital et al, 1989 ) . Perineurial macroglobulin deposition has been described ( Johnson et al, 1979 ) , although only 1 of these patients had a circulating IgM paraprotein, and deposition of IgA, IgG and IgM subclasses occurred, suggesting passive transfer rather than specific immune binding.…”

Section: Discussioncontrasting

confidence: 53%

Microvasculitic paraproteinaemic polyneuropathy and B‐cell lymphoma

Turner

Warren

Jacobs

et al. 2003

J Peripheral Nervous Sys

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Microvasculitis may play a greater part in the pathogenesis of paraproteinaemic neuropathies than is generally recognised, producing tissue destruction by convergent immune and physical mechanisms. We present a patient with a clinical syndrome of mononeuritis multiplex and a circulating IgM lambda paraprotein, in whom bone marrow aspiration revealed a lymphoplasmacytoid lymphoma. Microvasculitic changes were present in the first nerve biopsy, and the second showed extensive destruction of neural architecture and deposition of IgM-related material. A 2-stage pathogenic cascade is postulated and explored with a review of the relevant literature.

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Section: Discussioncontrasting

confidence: 53%

Microvasculitic paraproteinaemic polyneuropathy and B‐cell lymphoma

Turner

Warren

Jacobs

et al. 2003

J Peripheral Nervous Sys

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“…Part of the myelin widening process includes the increased separation of terminal loops in the paranodal region (Jacobs and Scadding, 1990). First demonstrated by Sluga (1970), wide myelin has been a consistent finding in IgM paraproteinaemic neuropathy both of malignant (Propp et al, 1975) and benign type (Jacobs and Scadding, 1990;Lach et al, 1993;Monaco et al, 1990;Meier et al, 1984;Mendell et al, 1985;Smith et al, 1983;Vital et al, 1989;Yeung et al, 1991) and may be considered as almost specific for these neuropathies (Vital et al, 1989). Widened myelin was also described in the experimental model of paraprotein neuropathy in the chick (Tatum, 1993) (see Experimental Studies).…”

Section: Pathology Of Neuropathymentioning

confidence: 94%

“…The incidence of wide myelin varies greatly from one case to another but may affect over 80% of myelinated fibres (Jacobs and Scadding, 1990). It is frequently observed in the outermost layers of the myelin sheath (Lach et al, 1993;Meier et al, 1984;Melmed et al, 1983;Pollard et al, 1985;Vital et al, 1989). A number of reports describe wide myelin in fibres that are probably remyelinating (Meier et al, 1984;Mendell et al, 1985).…”

Section: Pathology Of Neuropathymentioning

confidence: 99%

Morphological changes at paranodes in IgM paraproteinaemic neuropathy

Jacobs¹

1996

Microsc. Res. Tech.

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The paranode is one of a number of sites of a specific myelin sheath abnormality found in cases of IgM paraproteinaemic neuropathy. The gammopathy may be malignant or, more frequently, benign, and is often associated with a predominantly demyelinating neuropathy. The circulating paraprotein IgM antibody, usually with kappa light chains, was found in many cases to recognise an antigenic determinant in myelin, identified as myelin‐associated glycoprotein (MAG). Other glycoconjugates expressed by Schwann cells may also be recognised by the antibody. MAG is localized to regions of the myelin sheath in which the membranes are uncompacted. The paranode is one such region, and there is evidence that IgM is deposited specifically on the membranes of the terminal loops of the myelin sheath in addition to other MAG‐associated regions of the sheath. In many cases the presence of the paraprotein appears not to otherwise affect paranodal organization; in a few it is associated with changes to the termination of the loops on the axolemma and to the associated Schwann cell cytoplasm. These findings do not provide unambiguous evidence that binding of anti‐MAG IgM antibodies at the paranode is a direct cause of demyelination. Whilst localization of the paraprotein closely matches that of MAG, proof is still lacking that the relevant antigen is MAG itself. © 1996 Wiley‐Liss, Inc.

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“…Pathological studies in neuropathy with anti-MAG antibodies reveals demyelination (Fig. 2 ) in association with widening of myelin lamellae on electron microscopic examination [ 96 ] along with deposits of IgM and complement on myelin sheaths as demonstrated by direct immunohistochemistry (Fig. 2 ) [ 97 , 98 ].…”

Section: Pathological Studiesmentioning

confidence: 99%

An update on the diagnosis and management of the polyneuropathy of POEMS syndrome

Cerri¹,

Falzone²,

Riva³

et al. 2018

J Neurol

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POEMS syndrome is a rare, chronic, disabling paraneoplastic disorder characterized by peripheral neuropathy, organomegaly, endocrinopathy, monoclonal plasma cells disorder and skin changes. Diagnosis relies on the fulfillment of a set of clinical criteria of which polyneuropathy and a monoclonal plasma cell dyscrasia are early and essential features. Treatment may be either local or systemic and is aimed at the monoclonal plasma cell disorder. Our knowledge of the pathogenesis underlying the POEMS syndrome has advanced greatly over the past years, favoring an important progression in the recognition and management of this disorder. Here, we discuss the recent literature that has advanced our knowledge of the pathogenesis and clinical management of the polyneuropathy in POEMS syndrome.

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Polyneuropathy associated with IgM monoclonal gammopathy

Cited by 121 publications

References 29 publications

Microvasculitic paraproteinaemic polyneuropathy and B‐cell lymphoma

Microvasculitic paraproteinaemic polyneuropathy and B‐cell lymphoma

Morphological changes at paranodes in IgM paraproteinaemic neuropathy

An update on the diagnosis and management of the polyneuropathy of POEMS syndrome

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